Search results for "KINASE"

showing 10 items of 2635 documents

Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment

2014

A number of studies suggest that cancer stem cells are essential for tumour growth, and failure to target these cells can result in tumour relapse. As this population of cells has been shown to be resistant to radiation and chemotherapy, it is essential to understand their biology and identify new therapeutic approaches. Targeting cancer metabolism is a potential alternative strategy to counteract tumour growth and recurrence. Here we applied a proteomic and targeted metabolomic analysis in order to point out the main metabolic differences between breast cancer cells grown as spheres and thus enriched in cancer stem cells were compared with the same cells grown in adherent differentiating c…

Cancer ResearchImmunologyPopulationPyruvate KinaseBreast NeoplasmsOxidative phosphorylationBiologyDeoxyglucoseOxidative PhosphorylationCellular and Molecular Neurosciencechemistry.chemical_compoundPYRUVATE-KINASE M2Cancer stem cellLactate dehydrogenaseCell Line TumorHumansGlycolysiseducationSettore BIO/10 - BIOCHIMICASettore MED/04 - Patologia Generaleeducation.field_of_studyL-Lactate DehydrogenaseCell growthTUMOR-GROWTHSettore BIO/12Cell BiologyCell biologychemistry2-deoxyglucose BCSCNeoplastic Stem CellsFemaleOriginal ArticleStem cellGlycolysisPyruvate kinase
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Moguntinones--new selective inhibitors for the treatment of human colorectal cancer.

2014

Abstract 3-Indolyl and 3-azaindolyl-4-aryl maleimide derivatives, called moguntinones (MOG), have been selected for their ability to inhibit protein kinases associated with angiogenesis and induce apoptosis. Here, we characterize their mode of action and their potential clinical value in human colorectal cancer in vitro and in vivo. MOG-19 and MOG-13 were characterized in vitro using kinase, viability, and apoptosis assays in different human colon cancer (HT-29, HCT-116, Caco-2, and SW480) and normal colon cell lines (CCD-18Co, FHC, and HCoEpiC) alone or in combination with topoisomerase I inhibitors. Intracellular signaling pathways were analyzed by Western blotting. To determine their pot…

Cancer ResearchIndolesColorectal cancerAngiogenesisApoptosisBiologyPharmacologyMetastasisMaleimidesMiceIn vivomedicineAnimalsHumansPI3K/AKT/mTOR pathwayKinaseTOR Serine-Threonine Kinasesmedicine.diseaseXenograft Model Antitumor AssaysOncologyApoptosisSignal transductionCaco-2 CellsTopoisomerase I InhibitorsColorectal NeoplasmsHT29 CellsProto-Oncogene Proteins c-aktSignal TransductionMolecular cancer therapeutics
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Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses.

2009

Udgivelsesdato: 2009-Nov Targeting protein kinases as a therapeutic approach to treat various diseases, especially cancer is currently a fast growing business. Although many inhibitors are available, exhibiting remarkable potency, the major challenge is their selectivity. Here we show that the protein kinase CK2 inhibitors DMAT, TBB and resorufin differ in their selectivity against PI3K family members, since PI3K and DNA-PK are subject to inhibition by DMAT and TBB, however, not by resorufin. TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). In the case of resorufin no interference wit…

Cancer ResearchKinaseCell SurvivalBlotting WesternAntineoplastic AgentsCell cycleBiologyTriazolesCell killingOncologyBiochemistryApoptosisStress PhysiologicalCell Line TumorOxazinesPhosphorylationHumansBenzimidazolesViability assayCasein kinase 2Signal transductionCisplatinEnzyme InhibitorsCasein Kinase IISignal TransductionInternational journal of oncology
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Efficacy of BET Bromodomain Inhibition in Kras-Mutant Non–Small Cell Lung Cancer

2013

Abstract Purpose: Amplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion, and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that bromodomain and extra-terminal (BET) bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven non–small cell lung cance…

Cancer ResearchLKB1Lung NeoplasmsMutantApoptosisMYCAMP-Activated Protein KinasesProtein Serine-Threonine KinasesBiologyNSCLCmedicine.disease_causeArticleProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)MiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumorKRASmedicineAnimalsRNA Small InterferingLung cancerneoplasmsCell ProliferationMice KnockoutGene knockdownCell growthNuclear ProteinsCancerAzepinesTriazolesBETmedicine.diseaseMolecular biologydigestive system diseasesrespiratory tract diseasesBromodomainOncologyCancer researchRNA InterferenceKRASSignal TransductionTranscription FactorsClinical Cancer Research
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Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…

2012

Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…

Cancer ResearchLung NeoplasmsCombination therapyAfatinibGene ExpressionAdenocarcinoma of LungCell Growth ProcessesAdenocarcinomaAfatinibArticleErlotinib HydrochlorideMiceAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsEpidermal growth factor receptorLung cancerErlotinib HydrochlorideProtein Kinase InhibitorsSirolimusbiologymedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyTumor progressionDrug Resistance NeoplasmCancer researchbiology.proteinDisease ProgressionQuinazolinesErlotinibTyrosine kinasemedicine.drugTranscription FactorsCancer research
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Targeting transcriptional addictions in small cell lung cancer with a covalent CDK7 inhibitor.

2014

Small cell lung cancer (SCLC) is an aggressive disease with high mortality, and the identification of effective pharmacological strategies to target SCLC biology represents an urgent need. Using a high-throughput cellular screen of a diverse chemical library, we observe that SCLC is sensitive to transcription-targeting drugs, in particular to THZ1, a recently identified covalent inhibitor of cyclin-dependent kinase 7. We find that expression of super-enhancer-associated transcription factor genes, including MYC family proto-oncogenes and neuroendocrine lineage-specific factors, is highly vulnerability to THZ1 treatment. We propose that downregulation of these transcription factors contribut…

Cancer ResearchLung NeoplasmsTranscription GeneticMolecular Sequence DataAntineoplastic AgentsBiologyBioinformaticsArticleMiceSuper-enhancerDownregulation and upregulationCell Line TumorMedicineAnimalsHumansEnzyme InhibitorsneoplasmsTranscription factorRegulation of gene expressionbusiness.industryCell BiologyNeoplasms ExperimentalSequence Analysis DNASmall Cell Lung CarcinomaXenograft Model Antitumor AssayshumanitiesCyclin-Dependent Kinasesrespiratory tract diseasesHigh-Throughput Screening AssaysGene Expression Regulation NeoplasticOncologyCovalent bondCancer cellCancer researchNon small cellSmall Cell Lung CarcinomaCyclin-dependent kinase 7businessTranscription Factor GeneCDK12Transcription FactorsCancer cell
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Abstract B5: A BMP7 variant inhibits angiogenesis in vitro and in vivo in part by downregulating VEGFR2 and FGFR1 expression in endothelial cells.

2013

Abstract Glioblastoma multiforme (GBM), the most aggressive glioma, requires active angiogenesis for growth and survival. Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Previously, we demonstrated the use of a BMP7 variant (BMP7v) to differentiate glioblastoma stem-like cells (GSLCs) and significantly reduce their tumorigenic potential (Tate and Pallini et al. 2012). Using an in vitro co-culture endothelial cord formation assay, a surrogate of angiogenesis, and its cognate in vivo model, we investigated the role of BMP7v in VEGF, basic FGF (bFGF), tumor-driven a…

Cancer ResearchMatrigelbiologyAngiogenesisSMADFibroblast growth factorReceptor tyrosine kinaseEndothelial stem cellOncologyIn vivoMothers against decapentaplegic homolog 4Immunologybiology.proteinCancer researchMolecular Cancer Therapeutics
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Prognostic significance of interferon regulating factor 4 (IRF4) in node-negative breast cancer.

2014

620 Background: The transcription factor IRF4 (interferon regulating factor 4) regulates immunoglobulin class switch recombination as well as plasma cell differentiation. We examined the prognostic significance of IRF4 mRNA expression in node-negative breast cancer. Methods: Microarray based gene-expression data for IRF4 (204562_at) were analysed in four previously published cohorts (Mainz, Rotterdam, Transbig, Yu) of node-negative breast cancer patients not treated with adjuvant therapy (n=824). A meta-analysis of previously published cohorts was performed using a random effects model. Prognostic significance of IRF4 on metastasis-free survival (MFS) was examined in the whole cohort and in…

Cancer ResearchMicroarraybusiness.industrymedicine.diseaseBreast cancerOncologyInterferonPlasma cell differentiationImmunologyCancer researchmedicineAdjuvant therapyAurora Kinase Askin and connective tissue diseasesbusinessTranscription factorIRF4medicine.drugJournal of Clinical Oncology
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Breast cancer genome-wide association studies: there is strength in numbers.

2012

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-spe…

Cancer ResearchMultifactorial InheritanceSettore MED/06 - Oncologia MedicaPALB2PopulationMAP Kinase Kinase Kinase 1Single-nucleotide polymorphismGenome-wide association studyBreast NeoplasmsBiologyPolymorphism Single NucleotideGenetic linkageGeneticsSNPHumansGenetic Predisposition to DiseaseReceptor Fibroblast Growth Factor Type 2educationMolecular BiologyGeneCHEK2Geneticsbreast cancer GWASeducation.field_of_studyMicrofilament ProteinsHigh Mobility Group ProteinsCancer researchTrans-ActivatorsFemaleApoptosis Regulatory ProteinsReceptors ProgesteroneGenome-Wide Association StudyOncogene
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Absence of mutations in the activation loop and juxtamembrane domains of VEGFR-1 and VEGFR-2 gene in chronic myelomonocytic leukemia (CMML)

2012

Cancer ResearchMutationbiologyVEGF receptorsChronic myelomonocytic leukemiaKinase insert domain receptorHematologymedicine.diseasemedicine.disease_causelaw.inventionchemistry.chemical_compoundOncologychemistrylawDNA Mutational AnalysismedicineCancer researchbiology.proteinGeneDNAPolymerase chain reactionLeukemia Research
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